Tirofiban preserves platelet loss during continuous renal replacement therapy in a randomised prospective open-blinded pilot study 英文参考文献.docVIP
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Tirofiban preserves platelet loss during continuous renal replacement therapy in a randomised prospective open-blinded pilot study 英文参考文献
Available online /content/12/4/R111
Research
Open Access
Vol 12 No 4
Tirofiban preserves platelet loss during continuous renal
replacement therapy in a randomised prospective open-blinded
pilot study
Andreas Link1, Matthias Girndt2, Simina Selejan1, Ranja Rbah1 and Michael B?hm1
1Klinik für Innere Medizin III, Universit?tsklinikum des Saarlandes, Kirrberger Strasse, 66421 Homburg/Saar, Germany
2Klinik für Innere Medizin IV, Universit?tsklinikum des Saarlandes, Kirrberger Strasse, 66421 Homburg/Saar, Germany
Corresponding author: Andreas Link, link@med-in.uni-saarland.de
Received: 8 Apr 2008 Revisions requested: 16 May 2008 Revisions received: 16 Jun 2008 Accepted: 29 Aug 2008 Published: 29 Aug 2008
Critical Care 2008, 12:R111 (doi:10.1186/cc6998)
This article is online at: /content/12/4/R111
? 2008 Link et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introduction Approximately one third of all patients with
cardiogenic shock suffer from acute kidney injury. Percutaneous
coronary intervention, intra-aortic balloon pump, and continuous
renal replacement therapy (CRRT) require effective antiplatelet
therapy and anticoagulation, resulting in a high risk for platelet
loss and bleeding events. The reversible platelet glycoprotein
IIb/IIIa receptor inhibitor tirofiban was investigated to preserve
platelet number and activation in a prospective open-blinded
endpoint evaluation study.
endpoints were urea reduction, haemofilter life span, bleeding
events, and necessity for platelet transfusions.
Results In UFH-treated patients, the percentage of platelet-
monocyte aggregates significantly increased (P 0.001) and
consecutively platelet cell count significantly decreased (P
0.001). In con
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